Kawakage M, Sato K, Karasawa A
Department of Pharmacology, Kyowa Hakko Kogyo Co., Ltd., Shizuoka, Japan.
Jpn J Pharmacol. 1994 Jun;65(2):163-6. doi: 10.1254/jjp.65.163.
We studied the effect of KW-3635, a selective thromboxane A2 (TXA2)-receptor antagonist, on experimental glomerulonephritis. The glomerulonephritis was induced in mice by the administration of rabbit anti-mouse glomerular basement membrane (GBM) antibody. It was characterized as proteinuria, changes of serum biochemical parameters and glomerular histopathological abnormalities. The administration of KW-3635 (30 mg/kg/day, p.o.) significantly ameliorated the proteinuria, elevation of serum urea nitrogen and the thickening of GBM. These data suggest that TXA2 may play an important pathogenic role in the development and progression of glomerulonephritis.
我们研究了选择性血栓素A2（TXA2）受体拮抗剂KW-3635对实验性肾小球肾炎的影响。通过给予兔抗小鼠肾小球基底膜（GBM）抗体在小鼠中诱发肾小球肾炎。其特征为蛋白尿、血清生化参数变化和肾小球组织病理学异常。给予KW-3635（30毫克/千克/天，口服）可显著改善蛋白尿、血清尿素氮升高和GBM增厚。这些数据表明，TXA2可能在肾小球肾炎的发生和发展中起重要的致病作用。
